Painting by Matthias Grünewald of a patient suffering from advanced ergotism from approximately 1512–16 AD

Epidemics of the disease were identified throughout history, though the references in classical writers are inconclusive. Rye, the main vector for transmitting ergotism, was not grown much around the Mediterranean. When Fuchs 1834 separated references to ergotism from erysipelas and other afflictions, he found the earliest reference to ergotism in the Annales Xantenses for the year 857: "a Great plague of swollen blisters consumed the people by a loathsome rot, so that their limbs were loosened and fell off before death."

The blight, named from the cock's spur it forms on grasses, was identified and named by Denis Dodart, who reported the relation between ergotized rye and bread poisoning in a letter to the French Royal Academy of Sciences in 1676 (John Ray mentioned ergot for the first time in English the next year). "ergotism", in this modern sense, was first recorded in 1853; however, Sir Thomas Browne in his Christian Morals (published posthumously in 1716 although penned sometime in the 1670s) also made mention of 'ergotisms' .[2] Browne in turn, may have been introduced to the word through correspondence with John Ray.

Notable epidemics of ergotism occurred up into the 19th century. Fewer outbreaks have occurred since then due to rye being carefully monitored in developed countries. A severe outbreak of something akin to ergot poisoning occurred, however, in the French village of Pont-Saint-Esprit in 1951, resulting in five deaths.[3] The outbreak, and the diagnostic confusion surrounding it, are vividly described in John Grant Fuller's book The Day of St Anthony's Fire.[4]

When milled, the ergot is reduced to a red powder,[7] obvious in lighter grasses but easy to miss in dark rye flour. In less wealthy countries, ergotism still occurs; an outbreak in Ethiopia occurred in mid-2001 from contaminated barley. Whenever there is a combination of moist weather, cool temperatures, delayed harvest in lowland crops and rye consumption, an outbreak is possible.

Poisonings due to consumption of seeds treated with mercury compounds are sometimes misidentified as ergotism.[8][9] As Dr. Simon Cotton (member of the Chemistry Department of Uppingham School, UK) notes, there have been numerous cases of mass-poisoning due to consumption of mercury-treated seeds.[10]

Dark-purple or black grain kernels, known as ergot bodies, can be identifiable in the heads of cereal or grass just before harvest. In most plants the ergot bodies are larger than normal grain kernels, but can be smaller if the grain is a type of wheat. A larger separation between the bodies and the grain kernels show the removal of ergot bodies during grain cleaning.

Removal of ergot bodies is done by placing the yield in a brine solution; the ergot bodies float while the healthy grains sink.[11] Infested fields need to be deep plowed; ergot will not germinate if buried more than one inch deep and won't spread their spores in the air. Rotating crops, using non-susceptible plants, helps reduce infections since ergot spores only live one year. Rotation is an important part of managing ergot, since most cereal crops are sown with a "no-till" practice, where new crops are seeded directly into the stubble from the previous crop to reduce soil erosion.[12] Wild and escaped grasses and pastures can be mowed before they flower to help limit ergot infections.

Chemical controls can be used, but are not considered economical especially in commercial operations, and germination of ergot spores can still occur under favorable conditions.

The hypothesis that ergotism could explain cases of bewitchment has been subject to debate and has been criticized by several scholars. Within a year of Caporael’s article, the historians Spanos and Gottlieb argued against the idea in the same journal. In Spanos and Gottlieb’s rebuttal to Caporael’s article, they concluded that there are several flaws in the explanation of ergot poisoning as a cause of conditions associated with cases of alleged bewitchment. For example, they argued that, if the food supply was contaminated, the symptoms would have occurred on a house-by-house basis, not just in particular individuals. Historian Leon Harrier has challenged this theory by claiming that even if supplies were properly cooked, residents suffering from stomach ulcers had a risk of absorbing the toxin through the stomach lining, offering a direct route to the bloodstream. Being similar to Lysergic acid diethylamide (LSD), the chemical composition of the average human's stomach would be too acidic for the ergot to survive, especially if the food was properly cooked. But, if some residents were malnourished and suffering from bleeding stomach ulcers, there is valid reasoning to say that, while most of the residents would not be affected by ingesting contaminated grains, a small percentage could have become affected, offering an explanation for why ergotism was never initially recognized. Harrier has even argued that the numbers could have been exponentially larger, possibly even the entire town, but, due to the trials on bewitchment and heresy, and the fear of being accused and subsequently executed, few could come forward while suffering from legitimate medical conditions. Spanos and Gottlieb also state that ergot poisoning has additional symptoms not associated with the events in Salem and that the proportion of children afflicted were less than in a typical ergotism epidemic.[15] The anthropologist H. Sidky noted that ergotism had existed for centuries before the Salem witch trials, and argued that its symptoms would have been recognizable during the time of the Salem witch trials.[16]

More recently, it has been pointed out that ergots produced by different strains of Claviceps purpurea, and those growing in different soils, may have expressed different ergot alkaloid compositions. This may explain the different manifestations of ergotism in different outbreaks. For example, an alkaloid, present in high concentrations in ergots from Europe east of the Rhine, may historically have caused convulsive ergotism, while to the west it caused epidemics of gangrenous ergotism.[17]

^Cotton, Simon (October 2003), "Dimethylmercury and Mercury Poisoning", Molecule of the Month, UK: School of Chemistry, University of Bristol, More horrifying than this were epidemics of poisoning, caused by people eating treated seed grains. There was a serious epidemic in Iraq in 1956 and again in 1960, whilst use of seed wheat (which had been treated with a mixture of C2H5HgCl and C6H5HgOCOCH3) for food, caused the poisoning of about 100 people in West Pakistan in 1961. Another outbreak happened in Guatemala in 1965. Most serious was the disaster in Iraq in 1971–2, when according to official figures 459 died. Grain had been treated with methyl mercury compounds as a fungicide and should have been planted. Instead it was sold for milling and made into bread. It had been dyed red as a warning and also had warning labels in English and Spanish that no one could understand..